Knotted Solitons in a Charged Two-Condensate Bose System

By making use of the decomposition of U(1) gauge potential theory and the \phi mapping method, we propose that a charged two-condensate Bose system possesses vortex lines and two classes of knotted solitons. The topological charges of the vortex lines are characterized by the Hopf indices and the Brower degrees of \phi-mapping, and the knotted solitons are described by the nontrivial Hopf invariant and the BF action, respectively.Comment: 12 pages,0 figure

Generalized Froggatt-Nielsen Mechanism

In this paper, we propose a Generalized Froggatt-Nielsen mechanism in which non-renormalizable operators involving a GUT group and $U(1)_H$ non-singlet Higgs field are introduced. Thus the GUT gauge symmetry breaking and the generation of hierarchical flavor hierarchy have a common origin in this mechanism. In this Generalized Froggatt-Nielsen mechanism, we propose universality conditions for coefficients corresponding to different contractions in the group productions. We find that the predictions in Generalized Froggatt-Nielsen mechanism for SU(5) GUT is different to that of ordinary Froggatt-Nielsen mechanism. Such Generalized Froggatt-Nielsen mechanism can be used in GUT models when ordinary Froggatt-Nielsen mechanism is no longer available. We study the application of Generalized Froggatt-Nielsen mechanism in SO(10) model. We find that realistic standard model mass hierarchy and mixings can be obtained both in SU(5) and SO(10) GUT models with such Generalized Froggatt-Nielsen mechanism.Comment: 4 pages, no figure

NGF-TrkA signaling dictates neural ingrowth and aberrant osteochondral differentiation after soft tissue trauma

: Pain is a central feature of soft tissue trauma, which under certain contexts, results in aberrant osteochondral differentiation of tissue-specific stem cells. Here, the role of sensory nerve fibers in this abnormal cell fate decision is investigated using a severe extremity injury model in mice. Soft tissue trauma results in NGF (Nerve growth factor) expression, particularly within perivascular cell types. Consequently, NGF-responsive axonal invasion occurs which precedes osteocartilaginous differentiation. Surgical denervation impedes axonal ingrowth, with significant delays in cartilage and bone formation. Likewise, either deletion of Ngf or two complementary methods to inhibit its receptor TrkA (Tropomyosin receptor kinase A) lead to similar delays in axonal invasion and osteochondral differentiation. Mechanistically, single-cell sequencing suggests a shift from TGFβ to FGF signaling activation among pre-chondrogenic cells after denervation. Finally, analysis of human pathologic specimens and databases confirms the relevance of NGF-TrkA signaling in human disease. In sum, NGF-mediated TrkA-expressing axonal ingrowth drives abnormal osteochondral differentiation after soft tissue trauma. NGF-TrkA signaling inhibition may have dual therapeutic use in soft tissue trauma, both as an analgesic and negative regulator of aberrant stem cell differentiation

The Combined Effects of Amino Acid Substitutions and Indels on the Evolution of Structure within Protein Families

BACKGROUND: In the process of protein evolution, sequence variations within protein families can cause changes in protein structures and functions. However, structures tend to be more conserved than sequences and functions. This leads to an intriguing question: what is the evolutionary mechanism by which sequence variations produce structural changes? To investigate this question, we focused on the most common types of sequence variations: amino acid substitutions and insertions/deletions (indels). Here their combined effects on protein structure evolution within protein families are studied. RESULTS: Sequence-structure correlation analysis on 75 homologous structure families (from SCOP) that contain 20 or more non-redundant structures shows that in most of these families there is, statistically, a bilinear correlation between the amount of substitutions and indels versus the degree of structure variations. Bilinear regression of percent sequence non-identity (PNI) and standardized number of gaps (SNG) versus RMSD was performed. The coefficients from the regression analysis could be used to estimate the structure changes caused by each unit of substitution (structural substitution sensitivity, SSS) and by each unit of indel (structural indel sensitivity, SIDS). An analysis on 52 families with high bilinear fitting multiple correlation coefficients and statistically significant regression coefficients showed that SSS is mainly constrained by disulfide bonds, which almost have no effects on SIDS. CONCLUSIONS: Structural changes in homologous protein families could be rationally explained by a bilinear model combining amino acid substitutions and indels. These results may further improve our understanding of the evolutionary mechanisms of protein structures